The DOCK5 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the DOCK5 gene in the human SK-HEP-1 cell line. This product provides a heterogeneous pool of cells with targeted gene disruption, serving as a loss-of-function model for studying DOCK5-dependent biological processes. The polyclonal format allows for the analysis of knockout effects across a mixed genetic background, avoiding clonal artifacts while enabling robust functional genomics approaches.
SK-HEP-1 is a human hepatic adenocarcinoma cell line originally derived from the ascitic fluid of a patient with hepatic adenocarcinoma. This cell line exhibits an endothelial-like morphology and expresses markers characteristic of both endothelial and epithelial lineages, making it a valuable model for hepatocellular carcinoma progression and sinusoidal endothelium biology. SK-HEP-1 cells are widely employed to study the molecular mechanisms of liver cancer metastasis, angiogenesis, and the interaction between tumor cells and the vascular endothelium.
DOCK5 encodes a guanine nucleotide exchange factor (GEF) that specifically activates Rac1 by catalyzing GDP/GTP exchange. In complex with ELMO1/2, DOCK5 mediates Rac1 activation downstream of stimuli such as EGF, HGF, and integrin ??v??3. Activated Rac1 triggers phosphorylation of PAK1/2 and LIMK1, leading to cofilin inactivation and F-actin stabilization, thereby promoting lamellipodia formation and focal adhesion turnover. This pathway is critical for cell adhesion, migration, and invasion, with DOCK5 also modulating expression of MMP2 and MMP9 for matrix degradation.
In the SK-HEP-1 context, disruption of DOCK5 impairs the ability of these cells to activate Rac1 in response to migratory cues, resulting in reduced lamellipodia formation and diminished invasive capacity. Given that SK-HEP-1 cells are commonly used to model the metastatic behavior of hepatocellular carcinoma, DOCK5 knockout in this background provides a powerful tool to dissect the contribution of Rac1-dependent cytoskeletal remodeling to liver cancer metastasis. The polyclonal knockout population enables investigators to assess the heterogeneity of cellular responses to gene loss and to observe collective effects on cell behavior without the influence of clonal selection.
This product is suitable for investigating tumor cell migration and invasion, screening anti-metastatic drugs, and analyzing GEF function. Key assays include wound healing migration, transwell invasion, Rac1 activity pull-down, western blotting for phospho-PAK1/2 and phospho-LIMK, and F-actin immunofluorescence. It can also be used in xenograft metastasis models. For further details, contact Ascent Research.
